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Unit 5: LGS > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Normal physiology of gastric acid secretion

  • How is it produced
  • How is it secreted?
A
  • Formation

- Being pumped into lumen

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2
Q

What is secretion used for?

- How? Each macro?

A
  • Digestion.
  • Activates pepsinogen to pepsin to break down protein into AA
  • For fats use gastric lipase
  • Do not break down carbs in stomach
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3
Q

Why do we not chemically digest carbs in stomach

A

No, because amylase is not activated due to low pH (acidic) and it needs alkalinic pH.

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4
Q

What causes dysregulation of secretion?

- examples

A
  • Pathologies
    ○ Ulcers
    ○ Autoimmune diseases
    ○ Acute problem
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5
Q

Ulcers

  • kinds
  • cause
A
  • Gastric, Duodenal, Esophageal (usually more Gastric and Duodenal)
  • caused by H. pylori or chronic use of NSAIDS
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6
Q

How do you actually form the hydrogen

A
  • Inside the cell youre going to have CO2 and H2O then carbonic anhydrase is going to convert them to H2CO3 which then is broken down into hydrogen ions and bicarb.
  • The hydrogen will be pumped one way and then bicarb will be pumped the other way.
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7
Q

How to pump hydrogen ions into lumen

A

Proton pump, ATPase

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8
Q

What does ATPase mean

A

It needs energy and it is active transporter meaning something is going against its concentration gradient.

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9
Q

Proton pump

  • What is being pumped from the cell into the lumen?
  • What is pumped from the lumen to the cell?
A
  • Hydrogen

- Potassium

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10
Q

Where is chloride coming from? How does it enter the cell?

A
  • Blood

- Cl will be pumped into the cell and bicarb will be pumped out into the blood

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11
Q

Tri-transporter

  • other name
  • what does it transport
A
  • NKCC1

- Sodium, chloride, and potassium

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12
Q

Sodium potassium ATPase

A

○ Pumps sodium out and potassium in
○ Helps to keep everything electro neutral
- The more proton pumps you have, the more acid that can be secreted out

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13
Q

Potassium channels

A

allow for local gradients of potassium, which helps drive the proton pump

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14
Q

Parietal cells

  • function
  • what do they need?
  • what is being produced?
A
  • cells that secrete the acid, - need a lot of energy and have a lot of mitochondria in order to produce a lot of ATP so that ATPase’s can be functional.
  • both acids and bases are being produced.
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15
Q

Parietal cells

  • function
  • what do they need?
  • what is being produced?
  • How does cell not become basic?
A
  • cells that secrete the acid, - need a lot of energy and have a lot of mitochondria in order to produce a lot of ATP so that ATPase’s can be functional.
  • both acids and bases are being produced.
  • As it is pumping acid into lumen of stomach the bi-carb is being pumped into basolateral side, into the blood-stream. During digestion, especially gastric phase, when you are having secretion really activated there will be an alkaline tide.
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16
Q

Alkaline tide

A

high level of bi-carb in blood due to protons being pumped into lumen to make stomach acid. But blood will run through gastric mucousal so some of the excess bicarb in the blood can go into the gastric mucousal cells that it needs to be in and help to make the mucus layer.

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17
Q

What happens when an antacid is put into stomach?

- examples

A
  • Neutralizes HCl

- Calcium carbonate, Sodium bicaronate, Magnesium hydroxide, Aluminum hydroxide

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18
Q

Calcium carbonate

- When it reacts with hydrochloric acid what byproducts do you get

A
  • Calcium Chloride (CaCl2) and Carbon Dioxide (CO2)
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19
Q

Sodium bicarbonate

  • other name
  • When it reacts with hydrochloric acid what byproducts do you get
  • What happens when given to people with heart failure
A
  • Also known as baking powder or Alka-Seltzer
  • Sodium Chloride (NaCl) and Carbon Dioxide (CO2)
  • Increase water retention because salt will increase osmotic pressure.
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20
Q

Antacids and diarrheal agents/ antidiarrheals

A

○ Magnesium hydroxide: Magnifies diarrhea

○ Aluminum hydroxide: halts diarrhea

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21
Q

What happens because CO2 is produced with Antacids

A

Can get burping, belching, bloating because CO2 is gas. So if patient is belching frequently or very bloated after taking this medication it could be from CO2 production. However, CO2 is weak base which helps to neutralize the acid.

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22
Q

How do antacids affect other meds?

A
  • It reacts with them and reduces absorption

- It also affects solubility (Lipid/ Water)

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23
Q

What happens to pH with sodium bicarbonate and calcium bicarbonate?

A

being messed up so if a lot of antacids are being taken then you can get metabolic alkalosis.

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24
Q

surface mucousal cells

A

○ Secreting: bicarb and mucus

○ Turn over every 1 to 3 days

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25
Q

mucus neck cells

  • what are they
  • what do they become
A

○ Precursor stem cells
○ Can migrate up and become surface mucousal cells
○ Can migrate down and turn into ECL, parietal or chief cells
- There cells are important because top layer is being sloughed off every 1-3 days

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26
Q

Parietal cells

- what do they secrete?

A
  • Secrete HCl and intrinsic factor
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27
Q

D cells

- what do they secrete? and what does it do?

A

○ Secrete: somatostatin

- Turns things off

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28
Q

Enterochromafin like cells (ECL cells)

- what do they secrete?

A

Secrete histamine

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29
Q

Chief cells

- what do they secrete?

A

Secrete pepsinogen and gastric lipase

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30
Q

What cells are in the fundus and body of the stomach?

A

surface mucousal cells, mucus neck cells, parietal cells, d cell, ECL cells, chief cells

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31
Q

What cells are in the antrum of the stomach?

A

g cells and d cells

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32
Q

Potentiation

  • what is it?
  • what will it lead to?
A
  • How the different cells in the stomach regulate each other
  • regulate how much acid will be produced.
  • Any kind of regulation with Gq or Gs causes signaling cascade which activates the parietal cell and increases the amount of proton pumps on the parietal cell.
  • More pumps on apical membrane = more acid production in order to digest food
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33
Q

cells activated by vagal input

- what kind of receptors do they use?

A
  • Activation: all muscarinic (M3) receptor that stimulates through G-q
  • G cell activated by gastrin releasing peptide (GRP). which stimulates the G-cell to release gastrin.
  • Release of acetylcholine to activate parietal cells through a muscarinic receptor.
  • ECL cells: through ACH
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34
Q

cells inhibited by vagal input

A
  • D cell: uses ACH binding to m2/m4 muscarinic receptor to turn off somatostatin
    Don’t want somatostatin to be released when going through gastric phase of digestion
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35
Q

Gastrin

  • what kind of receptor?
  • cell released from
  • binds
A
  • Gq receptors
  • Released from G cell
  • Binds: CCK B receptor on ECL cell which in combination of acetylcholine helps to release histamine
    OR directly on parietal cells
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36
Q

Histamine

  • cells
  • what kind of receptor?
A
  • Chief cells, Parietal

- H2 receptor with G-s binding

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37
Q

How do chief cells and parietal cells work together for chemical digestion?

A
  • chief cells release pepsinogen and acid lipase. As pepsinogen is released into lumen it will be converted into pepsin by HCl. So the only way food can be broken down is through the release of hydrochloric acid
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38
Q

How does chemical digestion turn off? but how do we know when there has been enough gastric digestion so that we can turn it off?

A
  • Through somatostatin

○ CCK secretion from I cells in duodenum.

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39
Q

How is CCK turned on?

A

Fats and amino acids being released into duodenum from the food breaking down signals the I cells to release CCK. CCK effect on stomach is that it binds to CCK receptors to help slow down gastric digestion AND it causes release of somatostatin

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40
Q

PPIs

  • specific
  • how does it work?
  • Why do you have to give them multiple times?
  • pH
  • absorption
A
  • sodium potassium ATPase are only found in parietal cells so PPIs are very selective, most efficacious drug, most widely prescribed
  • irreversible covalent bond that forms and makes protein no longer functional. It’s required to be degraded and recycled, make new protein, which requires 3-5 days for new synthesis of this protein
  • because every time it is stimulated more PP are being upregulated to apical membrane. It’s a combination of recycled pumps and brand new pumps, so it takes 3-4 days in order for you to completely inactivate those proton pumps; If you were to remove proton pump inhibitor, it takes 3-4 days for you to get regular acid secretion again
  • weak bases (pKA is 4-5) in an acidic environment it will be protonatedand therefore ionized so it is donating protons; since it is charged it will be hydrophilic and trapped in the lumen
  • rapidly absorbed in the intestine because the pH will become more basic
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41
Q

Parietal cell resting vs secreting

- what happens with stimulation?

A
  • Resting state: Tubulovesicles that contain proton pump.
  • stimulation through potentiation: tubulovesicles combine with canniculus, so increases surface area of apical membrane and allows for up-regulation of proton pump
42
Q

Basal acid secretion

  • when does it occur?
  • mediated by?
A
  • going on during inter digestion (sleeping)
  • acid production is mediated by histamine, don’t have Ach and gastrin released at this time
  • Low level acid secretion to maintain sterility and regulated by histamine
43
Q

Cephalic Phase

  • what is happening
  • what is being released?
A
  • smell, see, taste, you’re starting to eat
  • You MUST consume it to continue this
  • You start to prime the pump.
  • You get some release of vagus and gastrin bc you’re anticipating the fact that you will have consumption occur
44
Q

Gastric Phase

A
  • You’re eating peristalsis occurs, gastric phase happens

- This is the potentiation: regulated by all 3 so you have high levels of it

45
Q

Intestinal Phase

A
  • bc of the acidity, amino acids and free fatty acids entering into the duodenum the I cells start to stimulate the release of CCK and this tell the stomach to slow down. As more and more gets into the intestinal phase, that’s when it slows down in the stomach to allow things to catch up.
  • You still have some acid secretion bc you still want to allow gastric phase to happen slowly in order to keep the digestion complete. However, start getting secretions of bicarb to try to neutralize the acid.
46
Q

lipid solubility

  • importance?
  • lipophilic drugs and solubility
A
  • helps the drugs to penetrate the cell membrane (phospholipid bilayer)
  • More lipophilic drugs are usually less water soluble
  • Ionized drug is not lipophilic; but non-ionized drugs are lipophilic
47
Q

PKA importance to drugs

A
  • doesn’t tell you if the drug is an acid or base, but it tells you the strength of the acidity or the strength of how basic the drug is
48
Q

Pharmacology and physiology

- Potential mechanisms to take advantage of?

A
  • H2 antagonists: will antagonize histamine receptors

- Proton pump: PPI will inhibit the proton pump

49
Q

Why is pH important for medications?

- Henderson Hasselbach

A
  • Ionization status is important for solubility and absorption
  • proportion of molecules of drug that were ionized to unionized
50
Q

Ion and lipophilicity

  • unionized
  • ionized
A
  • unionized drug is more liphilic
  • ionized drug is less lipophilic because it it more polar which will make it more likely to interact with water (hydrophilic) and won’t be able to penetrate cell very well (lipophobic)
51
Q

PKA and drugs

A
  • does not tell you if the drug is an acid or a base but tells you the strength of the acidity or the strength of basicity
52
Q

So if an acid has a pKA of 3.5 (aspirin), and the stomach pH is 1, will this drug be readily absorbed or not?
- how?

A
  • Weak acids and drugs are more readily absorbed in more acidic environments
  • When a weak acid is protonated (in an acidic environment), you have more unionized molecules than ionized; so since the pH is less than pKA the protonated version of the drug will be in its unionized form, and will be lipophilic.
53
Q

basic drugs in alkaline environment

A
  • More basic drugs are absorbed/more lipid soluble in an alkaline environment
54
Q

ph and ionization

  • weak acid
  • weak base
A
  • If it is a weak acid, the protonated form is unionized

- If it is a weak base, the protonated form is ionized

55
Q

PPI vs H2 antagonists and acidity graph

  • pre-treatment with H2
  • pre- treatment with PPI
  • Nocturnal acid secretion treatment
  • meal stimulated secretion
A

-H2: significant reduction in the amount of acid production throughout the day (especially with meal time) and also nocturnal acid production
PPI: almost complete abolishment of the response
- Nocturnal acid secretion more of an H2 mediated mechanism but you can also used PPIs for nocturnal secretion as well
- Meal stimulated secretion, H2 antagonist less effective than PPI bc with PPI you’re inhibiting all the way at the terminal step (the ATPase). The H2 antagonist still allows Ach and gastrin to allow release of acid
While histamine can try to blunt this effect, you still have the other molecules potentiating the release of the acid

56
Q

Four pharmacokinetic properties of PPIs that contribute to their efficacy

A
  • weak bases so they are rapidly absorbed in the intestine
  • Enteric coating of PPI prevents it from being broken down in high acidity of stomach and allows it to pass to intestine where it can be readily absorbed and trap the proton pump (drugs are not acting directly in stomach, they have to go into blood, penetrate through the cell to have action )
  • Canniculus is where all the protons are being pumped out, so you have increased acidity and pH is pretty low here. Having that increased acidity actually concentrates the ion trapping. It traps the proton pump inhibitor closer to its site of action which also increases its therapeutic effect
57
Q

PPI’s are prodrugs

A
  • Prodrugs are protected from first pass metabolism
  • Activated within the canaliculi of the parietal cell (the acidic environment there allows it to become their active metabolite)
58
Q

How to protect the parietal cells and mucosa from being degraded in the very acidic environment in lumen of stomach?

  • how?
  • what controls mucous layer?
A
  • Create buffer zone (mucous membrane)
  • Surface neck mucosa cells produce mucins that expand out and phospholipids, which creates very viscous protective barrier on top of the mucosa cells so they don’t get degraded by the acid
  • Prostaglandins ; stimulate blood flow to mucosal layer, induce secretion of bicarb and mucins to help create viscous layer, and helps repair mucosal cells if damaged/ renew or repair mucosal cells
59
Q

Prostaglandins other effects

- parietal cells

A
  • inhibit acid secretion

- Induces inflammatory response

60
Q

Mucosal protective agents

A
  • Sucralfate
  • Misoprostol
  • Bismuth subsalicylate
61
Q

Sucralfate

  • what is it?
  • charge?
  • how does it work?
  • when is it used?
A
  • Sucrose complex aluminum hydroxide compounds
  • Negatively charged,
  • Creates a barrier to protect from ulcers
  • Used as prophylaxis
62
Q

Misoprostol

  • what is it? why is that important?
  • when is it used?
A
  • PGE1 analogs(PGE1 important for mucosal health within GI )

- Prophylaxis for someone who may induce an NSAID induced ulcer

63
Q

Bismuth subsalicylate

  • other name?
  • what does it do?
A

Pepto bismol

- Have antibiotic properties, mucosal properties, and anti diarrheal

64
Q

H. pylori

  • what does it do to mucousal layer?
  • why?
  • what happens with the acid?
A
  • secretes urease which breaks down urea to ammonium and that breaks down the mucosal laye
  • protects the bacteria from the acid and allows them to start colonizing
  • acid going into walls of the stomach
65
Q

Gastric vs duodenal ulcer

  • how do they start?
  • what happens to feedback?
  • difference?
  • presentation
  • treatment
A
  • H. Pylori infection, inflam at level of antrum-G cells and D cells which causes decrease in somatostatin response and get a huge increase in gastrin which causes increase in acid secretion
  • overtime you get more acid secretion bc starts to break down duodenal mucosal cells and you lose feedback
  • duodenal ulcer you constantly have a hyper acid production bc doesn’t turn itself off. With gastric ulcer, you start to break down some of the body and fundus so start disrupting parietal cells and get more of a hypo secretion of acid later on
  • Duodenal ulcer-patient presents with epigastric pain that improves with meal; Gastric ulcer-pain worsens when meal occurs
  • Bismuth compounds. Some have antibiotic directly in them, alternatively they’re often paired with antibiotic like tetracycline
66
Q

NSAID and ulcers

- what does it inhibit? How can that cause an ulcer?

A
  • NSAIDs inhibit prostaglandins which stimulate blood flow to mucosal layer and help regenerate mucousal cells so NSAIDS will inhibit blood flow, prevent mucous layer being produced, and prevent repair of mucosal cells, so bc of this you’re having a high acid environment
  • will usually only produce a gastric ulcer
67
Q

autoimmune disease that disrupts parietal cells

A
  • another form of chronic gastritis. You can get disruption of parietal cells bc auto antibodies against them, gastrin, or intrinsic factor. Occurs in both fundus and body.
68
Q

Zollinger Ellison-tumor

A
  • one or more tumors form in your pancreas or the upper part of your small intestine
  • secrete large amounts of the hormone gastrin, which causes your stomach to produce too much acid. The excess acid then leads to peptic ulcers, as well as to diarrhea and other symptoms
69
Q

What is the GI tract for

A
  • To get nutrients into your body - they have to be broken down and absorbed. Together all of that is assimilation
70
Q

What is malabsorption

A
  • Bad absorption in the sense of some sort of inadequacy

It’s not about taking in the wrong things, it’s about not being able to take in the right things or in the right amounts

71
Q

Where are nutrients going to be absorbed?

A
  • In the small intestine: duodenum, jejunum, ilium
72
Q

Monosaccharide absorption

  • SGLT1
  • GLUT5
  • GLUT 2
  • Proton pump
A
  • SGLT1: on apical side of cell; transports Na and Glucose/galctose into the cell
  • GLUT5: on apical side of cell; transports fructose into the cell
  • GLUT2: On basolateral side of cell; transports glucose/galactose/and fructose out of cell to be transferred into blood
  • Proton pump: wi
73
Q

population related with loss of glucose and galactose transporters?

A
  • It’s rare, but more common in Amish populations
74
Q

enteral feeding

A

○ The normal way through the GI system; the normal way that we take in nutrients

75
Q

parenteral feeding

A

○ Anything outside of that normal way

example, putting it directly into a vein

76
Q

Malabsorption

  • definition
  • clinical presentation
  • what occurs chronically?
  • types pf chronic disorders?
A
  • defective absorption of fats, fat and water soluble vitamins, proteins, carbs electrolytes, minerals and water
  • chronic diarrhea, steatorrhea (fecal fat and bulky/frothy/greasy yellow or gray colored stools
  • weight loss, anorexia, abdonminal distention, borborygmi, and muscle wasting
  • pancreatic insufficiency, celiac disease and chrons disease
77
Q

short bowel syndrome

  • what molecules will be malabsorbed after resection of the ileum?
  • what can still be absorbed?
  • what other conditions could be caused?
  • what will the jejunum do?
  • what will happen to PT and PTT?
A
  • Vitamin B12, bile acids, fats, and proteins;
  • fats and proteins with the first section of the small intestine but not as much
  • anemia: B12 deficiency: macrocytic, normochromic
  • hyperplasia: will increase the number of cells which will lengthen the villi
  • should increase because of malabsorption of bile silts and therefore fat and fat soluble vitamins cannot be broken down so vitamin will be depleted
78
Q

What do the different sections of the bowel absorb?

A
  • duodenum: iron, calcium, carbs, fat and protein
  • jejunum: carbs, fat and protein
  • ileum: bile salts, vitamin B12, fats and proteins
79
Q

During bowel transplantation, which branch(es) of the aorta must be identified and anastomosed to supply blood to the jejunum, ileum, and ascending colon?

A
  • Superior mesenteric artery; which supplies blood from proximal jejunum to proximal transverse colon
80
Q

How might octreotide, a somatostatin analog, be used in small bowel resection?

A
  • will inhibit the release of gastrin to reduce gastric secretions and help slow down absorption to allow for more things to be absorbed
81
Q

Other blood supply in GI

A
  • celiac trunk: stomach, liver, spleen and duodenum

- inferior mesenteric: distal transverse colon, descending colon, and sigmoid colon

82
Q

Types of digestion

A
  • luminal, membrane, and intracellular
83
Q

Intraluminal digestion

A
  • When proteins, carbs, and fats are being broken down inside lumen of the GI tract into forms suitable for digestion
  • There is stuff that is released into that lumen that is meeting up with that food and causing digestion, and then it has to be assimilated (assimilation is digestion + absorbance)
84
Q

Terminal digestion

A
  • There are enzymes that sit on the brush border that help with enzymatic digestion
  • involves the hydrolysis of carbohydrates and peptides by disaccharidases and peptidases in the brush border of the small intestinal mucosa
85
Q

Transepithelial transport

A
  • epithelial have to be able to absorb them, and they do the absorbance through transport
  • membrane molecules that are positioned on the surface of epithelial cells to bring specific molecules into the cell
  • nutrients, fluid, and electrolytes are transported across and processed within the small intestinal epithelium
86
Q

Lymphatic transport

A
  • transport of absorbed lipids in the lymph
87
Q

primary bile acid malabsorption

  • What macronutrients will they help deal with digestion
  • types
A
  • malabsorption part means that they can’t absorb or get it in, can’t get bile acid
  • Digestion of lipids and fats
  • primary (genetic); secondary (acquired; ex. having part of ileum removed)
88
Q

Saliva

  • function
  • components
  • relation to GERD
A
  • lubricate, begin breakdown, and provide lumen alkaline; which helps against bacteria as well as neutralize acids until it reaches the stomach
  • water, HCO3, NA/K/CL and other ions, enzymes, immunoglobulins, and mucins
89
Q

Exocrine pancreatic secretions

- components

A
  • water, HCO3, NA/K/CL and other ions, enzyme, and mucins
90
Q

Hepatic caclicular secretions

  • what are they?
  • components
  • what will they merge and form?
A
  • thin tube that collects bile secreted by the hepatocyte
  • water, HCO3, ions, urea, AA, glucose, GSH bile acids, phosphatidylcholine, conjugated bilirubin, and xenobiotics
  • bile ductules which will become the common hepatic duct
91
Q

Secretory epithelial cells forming fluid

  • What major ion is put into the lumen by the cell to drive fluid into the lumen
  • What transporters are used to load the cell with the major ion
  • What mechanism is used to power the ion movements
  • What intracellular messengers are used to regulate the ion flow?
  • What pathway does water take into the lumen?
  • How is this process signaled/regulated?
A
  • Chloride, CFTR, and other chloride channels move the Cl- into the lumen
  • NKCC on basolateral membrane
  • Na+K+ ATPase:
  • j
  • Aquaporins or Paracellularly (from between the cells) through the process of osmosis
  • cAMP and Ca++ which can be signaled by Acetylcholine released from Vagal afferents
92
Q

NKCC

  • what does it transport?
  • where?
  • what does it do to intracellular charge?
  • how does it affect the transporter?
A
  • Na-K-Cl Cotransporter
  • basolateral membrane
  • more positive ions coming in than negative and chloride will leave the cell and enter the lumen so the intracellular charge will be more positive.
  • makes getting more positive ions into the cell through this transporter harder. It also makes getting Cl- out of the cell harder.
93
Q

Na+K+ ATPase

  • What is cell transporting?
  • where did it come from?
A
  • 2K+ in and 3Na+ out

- Remember the intracellular Na+ that is moving out originally came from the NKCC transporter

94
Q

Water pathway into the lumen

A

Chloride is secreted into the lumen via CFTR/chloride channels–> Na+ follows chloride–> water follows sodium by osmosis–> achieved water movement into the lumen

95
Q

Pancreatic, salivary, and hepatobiliary epithelial cells differences when producing fluid in secretory epithelial cells

A
  • in pancreas the acinar cells release enzymes and produce/secrete fluid to help move the fluid in/out of the duct
  • in salivary gland the secretory unit is called a salivon
  • in hepatobiliary tree hepatocytes are acting like acinar cells and are secreting enzymes into the lumen which then moves into the duct which is lined with Glandulocytes modify the fluid as it passes through
96
Q

How does pancreatic duct add bicarb to the luminal solution?

  • how is bicard in the pancreas cells?
  • how is bicarb released?
  • Where is the lumenal concentration of chloride being produced
A
  • Bicarbonate made by carbonic anhydrase within the cell using water and carbon dioxide. The products of this reaction include bicarb and hydrogen or can be brought into the cell from the blood via sodium-bicarb co-transporter (being powered by the concentration gradient achieved by Na+K+ ATPase)
    • The bicarb is released into the lumen via chloride exchanger on the apical side
  • Via CFTR (cystic fibrosis transmembrane conductance receptor) on the apical membrane
97
Q

CFTR: cystic fibrosis transmembrane conductance receptor

- regulator

A
  • cAMP is the regulator of this pump.
  • made by adenylate cyclase, and is modified by Gαi (inhibitory) and Gαs (stimulatory) receptors. These receptors are activated by hormones which is ultimately how all of this is being controlled/regulated.
98
Q

What is the result of the pH within the cell after bicarb is pumped out into the lumen?

  • where is H+ pumped? why?
  • won’t this alter pH of the blood
A

○ pH will decrease
○ hydrogen ions need to be pumped out basolaterally because it is bad for intracellular enzymes
- No because the volume/concentration of the cell vs volume/concentration of the blood is vastly smaller.

99
Q

CCK effects

  • Gallbladder
  • Pancreatic
  • Stomach activity
  • Sphincter of Oddi
A
  • Gallbladder contraction will increase bile
  • Pancreatic effect would be to release juice
  • Stomach activity will be decreased because a bolus from the stomach was just released into the duodenum which triggered CCK production.
  • Sphincter of Oddi (located where the pancreatic duct releases bile juices into the duodenum) will relax to allow secretion of bile.
100
Q

template for regulation of GI

  • Variable
  • Function
  • Stimulus
  • Sensor
  • Control center
  • Mediator
  • Effector
A

○ Variable= could be things like pH, nutrients, electrolytes
- Function= to achieve a certain pH, nutrient level, etc
○ Stimulus= something that triggers a change such as a change in pH after a meal
○ Sensor= detects the change in variable
○ Control center= determines what is a “normal” set point for core temperature/desired pH/etc
○ Mediator= signal that is sent by the control center wen the variable does not equal the set point (could be a neurotransmitter from a nerve or a hormone being secreted)
○ Effector= Usually an effector organ that releases another mediator that goes on to act on the appropriate tissue to bring the variable back to norma

101
Q

regulation of bicarb secretion.

  • what kind of feedback?
  • Variable
  • Sensor and controller
  • Mediator
  • Effector
  • Mediator #2
  • how much bicarb is produced?
A
  • negative feedback loop, meaning the product downregulates the cascade.
    ○ Variable= pH in the duodenum (is being decreased by acid)
    ○ Sensor and controller= S cells
    ○ Mediator= Secretin released by S cells–travels through blood to pancreatic duct
    ○ Effector= Pancreatic ducts
    ○ Another mediator= HCO3- which causes the pH to come back up
  • depends upon how acidic the lumen of the duodenum is moment to moment. The more acidic it is, the more secretin will be released into the blood. As the pH starts to increase due to bicarb production, the amount of secretin is tapered off.
102
Q

Regulation of CCK secretion in duodenum

  • variable:
  • sensors
  • controller
A
  • vol and nutrition of food bolus

- stretch and fat/protein

Unit 5: LGS (5 decks)

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